Dissociation of force decline from calcium decline by preload in isolated rabbit myocardium |
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Authors: | Michelle M Monasky Kenneth D Varian Jonathan P Davis Paul M L Janssen |
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Institution: | (1) Department of Physiology and Cell Biology, College of Medicine, The Ohio State University, 304 Hamilton Hall, 1645 Neil Avenue, Columbus, OH 43210-1218, USA |
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Abstract: | It is well known that the rate of intracellular calcium (Ca2+]i) decline is an important factor governing relaxation in unloaded myocardium. However, it remains unclear to what extent,
under near physiological conditions, the intracellular calcium transient amplitude and kinetics contribute to the length-dependent
increase in force and increase in duration of relaxation. We hypothesize that myofilament properties rather than calcium transient
decline primarily determines the duration of relaxation in adult mammalian myocardium. To test this hypothesis, we simultaneously
measured force of contraction and calibrated Ca2+]i transients in isolated, thin rabbit trabeculae at various lengths at 37°C. Time from peak tension to 50% relaxation (RT50(tension)) increases significantly with length (from 49.8 ± 3.4 to 83.8 ± 7.4 ms at an Ca2+]o of 2.5 mM), whereas time from peak calcium to 50% decline (RT50(calcium)) was not prolonged (from 124.8 ± 5.3 to 107.7 ± 11.4 ms at an Ca2+]o of 2.5 mM). Analysis of variance revealed that RT50(tension) is significantly correlated with length (P < 0.0001). At optimal length, varying the extracellular calcium concentration increased both developed force and calcium
transient amplitude, but RT50(tension) remained unchanged (P = 0.90), whereas intracellular calcium decline actually accelerated (P < 0.05). Thus, an increase in muscle length will result in an increase in both force and duration of relaxation, whereas
the latter is not primarily governed by the rate of Ca2+]i decline. |
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Keywords: | Preload Myofilament Calcium |
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